Mineralocorticoid Receptor-Mediated Sodium Retention
Fludrocortisone is a synthetic corticosteroid with predominant mineralocorticoid activity. [1]
Cellular Receptor Binding
Fludrocortisone diffuses into cells and binds the cytosolic mineralocorticoid receptor. [1] The fludrocortisone–receptor complex translocates to the nucleus and alters gene transcription. [1]
Renal Effects
In the distal nephron and collecting duct, increased transcription promotes apical sodium entry and basolateral sodium reabsorption. [1] This results in increased sodium reabsorption and increased extracellular fluid volume through secondary water retention. [1]
Electrolyte and Acid-Base Effects
Mineralocorticoid signaling increases urinary potassium secretion, which increases the risk of hypokalemia. [1] Mineralocorticoid signaling also increases hydrogen ion secretion, which can contribute to metabolic alkalosis. [1]
Endocrine Context
Because fludrocortisone has mineralocorticoid activity, it replaces or augments aldosterone-like effects in conditions with impaired mineralocorticoid function. [1]